OSBPL5 Knockout Raji Polyclonal Cells are a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphoblast cell line. This product offers a heterogeneous pool of cells with targeted disruption of the OSBPL5 gene, providing a physiologically relevant loss-of-function model for studying oxysterol-binding protein-like protein 5 (OSBPL5) in a B-cell lymphoma context. The polyclonal format preserves population-level diversity while ensuring robust reduction of OSBPL5 function, making it suitable for functional genomics screens and pathway analysis without the need for single-cell cloning. CRISPR/Cas9-mediated gene disruption introduces loss-of-function alleles across the cell population, enabling researchers to interrogate OSBPL5-dependent processes in a lymphoma-relevant background.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblastoid line, widely used as a model for human B-cell malignancies. These cells maintain key characteristics of activated B lymphocytes, including surface immunoglobulin expression and growth factor independence, and recapitulate aspects of lymphomagenesis driven by viral and oncogenic signals. As an established model for lymphoma research, Raji cells are amenable to genetic manipulation and serve as a robust platform for dissecting signaling pathways and metabolic dependencies that support B-cell transformation and survival.
OSBPL5 encodes a lipid transfer protein that localizes to endoplasmic reticulum?Cplasma membrane contact sites, where it mediates non-vesicular exchange of cholesterol and phosphatidylinositol 4-phosphate (PI4P). Through its FFAT motif, OSBPL5 binds the ER-resident VAPA and VAPB proteins, while its ORD domain interacts with PI4P at the plasma membrane. This dual interaction facilitates counter-directional transport, supplying cholesterol to the plasma membrane while removing PI4P for ER-localized metabolism. OSBPL5 is regulated downstream of SREBP transcription factors and cellular cholesterol levels, and in turn influences mTORC1 signaling, SREBP activation, and actin cytoskeleton organization. Loss of OSBPL5 disrupts cholesterol and PI4P homeostasis, leading to aberrant lipid distribution and impaired activation of downstream signaling cascades, including mTORC1-mediated phosphorylation of S6K and 4E-BP1.
In the Raji lymphoma context, OSBPL5 knockout is anticipated to perturb lipid trafficking critical for malignant B-cell proliferation and survival. Lymphoma cells often exhibit altered cholesterol metabolism to support membrane biogenesis and signaling platforms, and dysregulation of ER?Cplasma membrane contact sites may contribute to oncogenic processes. The OSBPL5 knockout Raji polyclonal cells therefore provide a tractable system to investigate how lipid exchange defects impact B-cell lymphoma biology, including mTORC1-driven anabolism, cytoskeletal remodeling, and apoptotic sensitivity. This model offers a unique opportunity to explore the intersection of lipid homeostasis and cancer cell fitness in an EBV-transformed background.
Researchers can employ these cells in a variety of functional assays to elucidate OSBPL5 biology and therapeutic vulnerabilities. Typical applications include Western blotting to confirm OSBPL5 loss, filipin staining to assess cholesterol distribution, PI4P immunofluorescence for contact site integrity, and mTORC1 pathway phospho-signaling analysis (e.g., p-S6K, p-4E-BP1). Additional phenotypic readouts encompass proliferation and apoptosis assays under lipid-modified conditions, RNA-seq profiling of cholesterol- and lipid-related gene networks, and mass spectrometry-based lipidomics. These tools support investigations into lipid transport mechanisms, cholesterol homeostasis in B-cell lymphoma, mTORC1 regulatory circuits, and drug target validation for lipid-dependent cancers. For additional information or technical support, please contact Ascent Research.
